While angiotensin is known to be an effective stimulus to aldosterone production, the role of the renin-angiotensin system in mediating the aldosterone response to sodium depletion is not firmly established. These studies are designed to evaluate the role played by angiotensin in regulating aldosterone production in the sodium-deplete rabbit. In acute studies, the nonapeptide inhibitor of angiotensin I converting enzyme, SQ 20881, will be administered to sodium deplete rabbits in order to determine whether acutely lowering the circulating concentration of angiotensin II affects the rate of aldosterone production. Similar acute studies will be performed during the passive administration of high titer rabbit antibodies against either angiotensin II or the 2-8 heptapeptide fragment ("angiotensin III"). In chronic studies, an attempt will be made to prevent the increase in plasma renin activity which characteristically occurs during dietary sodium depletion, by administration of propranolol throughout the period of sodium restriction in rabbtis. Parallel studies in normal volunteers and in patients with essential hypertension will attempt to answer the question whether the renin and aldosterone responses to sodium depletion may be dissociated. The finding that aldosterone production can increase independently of changes in the renin-angiotensin system would provide strong evidence for other factors controlling aldosterone production.